In completion of the previously outlined "experimental alcohol blastopathy", the role of acetaldehyde in the induction of preimplantation pathological changes in rat embryos has been controlled. Two experimental models were used: the direct administration of acetaldehyde by gavage and the blockage of acetaldehyde metabolization by ANTALCOL (an aldehyde-dehydrogenase blocking compound). The main results were as follows: The exogenous acetaldehyde in the blood of pregnant animals has an obvious effect upon the developmental rate during the late preimplantation period (retarding segmentation, blastulation), and in one of the experimental models upon the oviductal-uterine migration rate. The increase of the blood acetaldehyde level by blockage of its further metabolization has a more marked effect as compared with the direct intravenous administration of the substance. According to our previous observations the intravenous application of ethanol on the same day (day 4) has no such effect. The direct noxious influence upon the developing preimplantation embryos (fragmentation) of the increased level of acetaldehyde obtained by ANTALCOL treatment is similar but more marked than this effect obtained previously by ethanol administration. The same effect observed after the direct administration of the substance is less marked than the effect of ANTALCOL treatment but more marked than the effect of intravenous ethanol administration. These results attest that acetaldehyde may contribute (alone or together with the effect of ethanol) to the induction of "experimental alcohol blastopathy". The less marked action of the substance proper introduced into the blood stream may be due--in our opinion--to its possible alteration during the period between distillation and application.